This project is concerned with the pathogenesis of neonatal hypoglycemia in infants of diabetic mothers (IDM). The hypothesis is that insufficient hepatic glucose production, due either to increased liver sensitivity to insulin and/or diminished hepatic responsiveness to catabolic hormones, especially glucagon, is responsible for this hypoglycemia. Our studies will concentrate on hormonal receptor interactions in liver membranes and isolated hepatocytes from offspring of hyperglycemic rats. Furthermore, we will examine the effects of maternal hyperglycemia on neonatal hepatic glycogenolytic and gluconeogenic capacities.